Marital correlates of blood pressure.

In 1982, 1,260 white spouse pairs, aged 18 years and over, were interviewed as part of the Connecticut Blood Pressure Survey. The present report is based on a systematic analysis of 1) the personal characteristics and behavior of the spouse, 2) the roles and responsibilities of the material partners, and 3) similarity between spouses on selected variables. Results indicated that a number of these marital variables were associated with either systolic or diastolic blood pressure in husbands and in wives. Some components of the marital situation were associated with lower blood pressure whereas others were associated with higher blood pressure. Effects of marriage on blood pressure were observed both for husband's and wife's blood pressures, although the effects varied by sex. Similarity in spouses' behaviors and characteristics were more frequently associated with blood pressure than the individual effects of these behaviors. Age difference, measured as husband older than wife, was associated with lower blood pressure in husband's but with higher blood pressure in wives. Spouse's educational level and occupational status were not significantly related to blood pressure. Responsibility for common household chores (e.g., cooking) was associated with higher blood pressure in wives but responsibility for the family's health care was associated with lower blood pressure in both spouses.

Membrane abnormality of erythrocytes is highly dependent on salt intake and renin profile in essential hypertension: an electron spin resonance study.

The purpose of the present study was to investigate membrane fluidity in essential hypertension using electron spin resonance (ESR) and spin-labelling. Erythrocytes from patients with untreated essential hypertension were examined and compared with age-matched normotensive subjects. The values of outer hyperfine splitting (2T') and order parameter (S) of the ESR spectra for a fatty acid spin label agent (5-nitroxy stearate) were significantly higher in essential hypertension than in the normotensive subjects. However, these values were not changed in secondary hypertension. This finding indicates that the membrane fluidity of erythrocytes was lower in essential hypertension. Further, the abnormality was attenuated with low-salt intake, and, on the contrary, was more prominent with high-salt intake in essential hypertension. Calcium loading to erythrocytes in vitro caused a greater decrease in the membrane fluidity in essential hypertension than in the normotensive controls. This calcium-induced change in the membrane fluidity was significantly inversely correlated with the value of plasma renin activity in essential hypertension. These results suggest that abnormality in the membrane fluidity might be emphasized in the presence of calcium, especially in low-renin essential hypertension, implying enhanced calcium sensitivity in this type of hypertension.

Sodium sensitivity of blood pressure and baroreceptor reflex function in patients with essential hypertension.

In order to define the role of the baroreceptor reflex function in the sodium sensitivity of blood pressure in patients with mild essential hypertension, 25 patients were classified into two groups, salt-sensitive and salt-insensitive, depending on the difference in the averages of the resting systolic blood pressure, taken hourly on the fifth day of 7 days of sodium depletion and on the fifth day of 7 days of repletion. Increases in urinary sodium excretion and body weight and a decrease in haemotocrit during the sodium repletion period were similar in both groups. Baroreceptor reflex function, estimated from the baroreceptor slope and the blood pressure change on a 70 degrees tilting test, was enhanced by the sodium repletion period in the sodium-insensitive group but not in the sodium-sensitive group. These results suggest that sodium sensitivity might be due to differences in the ability of the baroreceptor reflex function to become sensitized during a high sodium intake.

Relationship of cellular calcium to salt sensitivity in patients with essential hypertension.

The significance of cellular calcium metabolism and systemic calcium balance in sodium chloride sensitivity was studied in 16 patients with essential hypertension and in 13 normotensive subjects. With changes in sodium chloride intake from 3 to 20 g/day, mean blood pressure, lymphocyte [Ca2+]i and the acute hypotensive response to nifedipine were increased in the hypertensive patients, but not in the normotensive subjects. Serum calcium concentration was decreased and urinary calcium excretion was increased in both groups. In the hypertensive patients, elevation of mean blood pressure was positively correlated with the increase in lymphocyte [Ca2+]i and with the enhancement of the hypotensive response to nifedipine, but it was not related to the change in serum or urinary calcium. These results suggest that enhancement of cellular-calcium-dependent vasoconstriction may lead to increased blood pressure following sodium chloride loading in patients with essential hypertension.

Sodium intake modulates left ventricular hypertrophy in essential hypertension.

In order to assess the impact of dietary sodium intake on the degree of left ventricular hypertrophy, we determined posterior wall thickness, relative wall thickness and left ventricular mass by two-dimensionally guided M-mode echocardiography, and related these parameters to sodium excretion over 24 h. There was no restriction on sodium intake. The first cohort comprised 43 subjects (residents of New Orleans) with mild to moderate essential hypertension who had not been treated for at least 4 weeks; in this cohort sodium excretion correlated with posterior wall thickness (r = 0.64, P less than 0.001), relative wall thickness (r = 0.67, P less than 0.001) and left ventricular mass (r = 0.37, P less than 0.02). A stepwise multiple regression analysis confirmed that sodium excretion was a determinant of posterior wall thickness (P less than 0.02) and relative wall thickness (P less than 0.05) independently of age, arterial pressure and body weight. The second cohort comprised 60 white male patients (residents of Bonn) with mild essential hypertension who had never been treated in the past; in this cohort sodium excretion correlated with diastolic diameter (r = 0.36, P less than 0.001) and with left ventricular mass (r = 0.35, P less than 0.001). Sodium excretion and systolic pressure emerged as independent variables (P less than 0.02) for left ventricular mass as evaluated by multiple regression analysis. These results identify dietary sodium intake as an independent powerful determinant of left ventricular hypertrophy in two disparate patient cohorts. Thus, for a similar haemodynamic load, sodium intake might accelerate, and conversely salt restriction mitigate, cardiac structural adaptation in patients with essential hypertension.

Dietary sodium restriction and blood pressure response to alpha-receptor blockade in young spontaneously hypertensive rats.

Dietary sodium restriction (9 mumol/g food) was started in 4-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), and was continued for 3 or 6 weeks. Low sodium intake for 3 weeks prevented the development of hypertension in SHR. More prolonged restriction caused hypotensive blood pressure levels in both SHR and WKY. At 7 weeks of age, SHR and WKY on a control diet showed similar blood pressure decreases after prazosin; at 10 weeks the response was significantly larger in SHR. Sodium restriction from 4 to 7 weeks of age did not inhibit the prazosin effect, whereas after more prolonged restriction the response was significantly inhibited in SHR compared with control SHR as well as with sodium-restricted WKY. These results indicate that sodium restriction may affect blood pressure in several ways, and that inhibition of the alpha 1-receptor mediated pressor effect is specific to SHR.

Relationship between the sympathetic nervous system and sodium potassium adenosine triphosphatase inhibitor in salt-sensitive patients with essential hypertension.

In order to evaluate endogenous Na+,K+-ATPase inhibitor on sympathetic nerve endings, endogenous Na+,K+-ATPase inhibitor and plasma noradrenaline were determined in patients with essential hypertension under different sodium conditions. Compared with the plasma from non-salt-sensitive patients, that from salt-sensitive patients showed significantly higher Na+,K+-ATPase inhibitor and plasma noradrenaline levels. Salt-induced changes in endogenous Na+,K+-ATPase inhibitor and those in blood pressure or plasma noradrenaline showed positive correlations. These results suggest that the salt-induced increase in endogenous Na+,K+-ATPase inhibitor might induce blood pressure elevation in essential hypertension, at least partly via increased noradrenaline levels.

Ouabainlike Na+,K+-ATPase inhibitor in the plasma of normotensive and hypertensive humans and rats.

Acute volume expansion, increased sodium intake, and restraint on sodium excretion endow the plasma with an increased capacity to inhibit sodium transport. Cytochemical techniques can detect the presence of Na+K+-adenosine triphosphatase (ATPase) inhibitor in the plasma of normal humans and rats, the concentration of which is controlled by salt intake. The substance responsible appears to originate in the hypothalamus, where the concentration is also controlled by salt intake. The plasma concentration of the cytochemically detectable Na+,K+-ATPase inhibitor is substantially raised in the plasma of patients with essential hypertension, spontaneously hypertensive rats (SHR) and of Milan hypertensive rats. The concentration of activity in the hypothalamus of SHR is also considerably raised. These findings demonstrate that these forms of hypertension are associated with a rise in the concentration of a cytochemically detectable circulating Na+,K+-ATPase inhibitor that under normal circumstances is controlled by salt intake.

Contribution of salt to arterial wall changes in DOCA hypertension in the rat.

The contribution of drinking fluid salt to the development of deoxycorticosterone (DOCA) hypertension and arterial wall changes was assessed in unilaterally nephrectomized rats. Half of the DOCA-treated animals received saline supplemented with 0.2% KCl and the other half received deionized water as drinking fluid. All animals were fed standard rat chow (Na content = 0.36%). After 8 weeks, arterial pressures were significantly elevated in both DOCA groups to values which were not significantly different. The heart weight to body weight ratio was also elevated in both DOCA groups with a larger response in the saline-treated ones. Body weight of saline-treated DOCA rats was significantly lower than untreated controls and water-treated DOCA rats. Arteries from both DOCA groups exhibited increased passive stiffness, larger maximum active stress, wall thickening, decreased collagen and elastin concentration, greater relative cell volume, and greater water and cation concentrations. Larger changes were generally found in the saline- than the water-treated group. These results show that saline administration is not necessary for the development of hypertension or hypertension-induced arterial wall changes in DOCA-treated, uninephrectomized rats. Hypertension developed more slowly and arterial wall changes were similar in magnitude in water-treated animals. These results suggest that the rate and/or time history of pressure elevation may be an important factor contributing to hypertension-related arterial changes.

Change in salt appetite due to rehydration level in rats.

Thermally dehydrated rats were given a choice of tap water and saline (0.9% or 1.8% NaCl), and the change in the salinity of their choice during rehydration was measured up to 15 hr. The rats consumed more water than saline for about 2 hr after the start of fluid replacement (about 55 mEq/l), while they consumed more saline than tap water (about 120 mEq/l) thereafter. Urine output and urinary Na output were only about 20% of their intake during the initial 4 hr of rehydration, while after 4 hr the output became almost equal with the intake. The change in salt intake occurred when about 90% of Na loss and 60% of fluid loss was regained. The results indicate that rats choose dilute salt solution to lower plasma osmolality during the initial period of the rehydration and then regain body fluid isotonically. Urine volume and urinary Na output increased only after volume repletion. Thus, osmoregulation with salt appetite has priority over fluid volume regulation in restitution from thermal dehydration.